The probability of developing cancer increases progressively with age in mammalian species. According to the multi-stage hypothesis of carcinogenesis, this marked dependence of cancer incidence rates on age may result from the prolonged exposure to environmental carcinogens that is necessary to produce the cellular mutations leading to malignancy. It follows from this hypothesis that shorter-lived species should be more susceptible to environmental carcinogens than longer-lived species. We have reported previously that in a cell-mediated assay for carcinogen activation employing cultured fibroblasts from six different mammalian species, there was a good inverse correlation between species life span and capacity of fibroblasts to activate DMBA to a mutagenic form (Exptl. Cell Res. 94, 445, 1975). We have since isolated three fibroblast strains from each of six mammalian species of widely differing life spans (rat, guinea pig, rabbit, cow, elephant, and human) and have found a good inverse correlation between species life span and the rate at which cultured fibroblasts bind 3H-DMBA to their DNA. BIBLIOGRAPHIC REFERENCES: Schwartz, A.G. Correlation Between Species Life Span and Capacity to Activate 7, 12-Dimethylbenz(a)anthracene to a Form Mutagenic to a Mammalian Cell. Exp. Cell Res. 94, 445 (1975).